ArticleThe Journal of experimental medicine1998
Transcription factor SCL is required for c-kit expression and c-Kit function in hemopoietic cells.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 76 citations in OpenAlex.
- Sodium butyrate supresses malignant human mast cell proliferation, downregulates expression of KIT and promotes differentiation.Frontiers in allergy · 2023Article
- Survivin is a novel transcription regulator of KIT and is downregulated by miRNA-494 in gastrointestinal stromal tumors.International journal of cancer · 2018Article
- SRC-like adaptor protein 2 (SLAP2) is a negative regulator of KIT-D816V-mediated oncogenic transformation.Scientific reports · 2018Article
- The adaptor 3BP2 is required for KIT receptor expression and human mast cell survival.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Silencing AML1-ETO gene expression leads to simultaneous activation of both pro-apoptotic and proliferation signaling.Leukemia · 2014Article
- Genetic interaction between Kit and Scl.Blood · 2013Article
- Article
- The expansion of T-cells and hematopoietic progenitors as a result of overexpression of the lymphoblastic leukemia gene, Lyl1 can support leukemia formation.Leukemia research · 2011Article
- Adenovirus-mediated stem cell leukemia gene transfer induces rescue of interstitial cells of Cajal in ICC-loss mice.International journal of colorectal disease · 2010Article
- Inhibition of all-trans retinoic acid-induced granulocytic differentiation of WEHI-3B D+ cells by forced expression of SCL (TAL1) and GATA-1.Leukemia research · 2009Article
- Selective enhancement of the uptake and bioactivity of a TAT-conjugated peptide inhibitor of glycogen synthase kinase-3.Molecular therapy : the journal of the American Society of Gene Therapy · 2009Article
- Adult hematopoietic stem and progenitor cells require either Lyl1 or Scl for survival.Cell stem cell · 2009Article
- Launching the T-cell-lineage developmental programme.Nature reviews. Immunology · 2008Review
- c-Jun homodimers can function as a context-specific coactivator.Molecular and cellular biology · 2007Article
- Functional but abnormal adult erythropoiesis in the absence of the stem cell leukemia gene.Molecular and cellular biology · 2005Article
- SCL assembles a multifactorial complex that determines glycophorin A expression.Molecular and cellular biology · 2004Article
- Altered transcription of the stem cell leukemia gene in myelofibrosis with myeloid metaplasia.Leukemia · 2003Article
- Translational control of SCL-isoform expression in hematopoietic lineage choice.Genes & development · 2003Article
- Establishing the transcriptional programme for blood: the SCL stem cell enhancer is regulated by a multiprotein complex containing Ets and GATA factors.The EMBO journal · 2002Article
- A single split-signal FISH probe set allows detection of TAL1 translocations as well as SIL-TAL1 fusion genes in a single test.Leukemia · 2002Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In normal hemopoietic cells that are dependent on specific growth factors for cell survival, the expression of the basic helix-loop-helix transcription factor SCL/Tal1 correlates with that of c-Kit, the receptor for Steel factor (SF) or stem cell factor. To address the possibility that SCL may function upstream of c-kit, we sought to modulate endogenous SCL function in the CD34(+) hemopoietic cell line TF-1, which requires SF, granulocyte/macrophage colony-stimulating factor, or interleukin 3 for survival. Ectopic expression of an antisense SCL cDNA (as-SCL) or a dominant negative SCL (dn-SCL) in these cells impaired SCL DNA binding activity, and prevented the suppression of apoptosis by SF only, indicating that SCL is required for c-Kit-dependent cell survival. Consistent with the lack of response to SF, the level of c-kit mRNA and c-Kit protein was significantly and specifically reduced in as-SCL- or dn-SCL- expressing cells. c-kit mRNA, c-kit promoter activity, and the response to SF were rescued by SCL overexpression in the antisense or dn-SCL transfectants. Furthermore, ectopic c-kit expression in as-SCL transfectants is sufficient to restore cell survival in response to SF. Finally, enforced SCL in the pro-B cell line Ba/F3, which is both SCL and c-kit negative is sufficient to induce c-Kit and SF responsiveness. Together, these results indicate that c-kit, a gene that is essential for the survival of primitive hemopoietic cells, is a downstream target of the transcription factor SCL.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.